Increased permeability of sheep lung vessels to proteins after Pseudomonas bacteremia

Brigham, Kenneth L.; Owen, Patty Jill; Bowers, Ronald E.

doi:10.1016/0026-2862(76)90067-4

Cited by 24 publications

(4 citation statements)

References 12 publications

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“…Hydroxyurea primarily depleted granulocytes; granulocyte depletion required [4][5][6][7][8][9][10][11] d. The effects of hydroxyurea on blood leukocyte and platelet counts are shown in Fig. 1.…”

Section: Resultsmentioning

confidence: 99%

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Prevention by granulocyte depletion of increased vascular permeability of sheep lung following endotoxemia.

Heflin¹,

Brigham²

1981

J. Clin. Invest.

394

116

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A B S T R A C T To see whether circulating granulocytes are necessary for the lung vascular reaction to endotoxin, we measured the endotoxin response in chronically instrumented sheep before and after granulocyte depletion with hydroxyurea. Granulocyte depletion did not affect the pulmonary hypertension caused by endotoxin (peak mean pulmonary artery pressures = 38+2 cm H20 before depletion and 42+2 after depletion, P = NS). The late phase increase in lung lymph flow after endotoxin was significantly lower in the granulocytopenic animals as reflected by lung lymph flow (mean steady state lymph flow before depletion = 30.6+2.0 SE ml/h; mean steady state lymph flow after granulocyte depletion = 15.4+1.0; P < 0.01) even though late phase pulmonary vascular pressures were similar before and after granulocyte depletion. Lung lymph protein clearance (lymph flow x lymph/plasma protein concentration) was also significantly lower after granulocyte depletion (mean steady state before depletion = 21.4 + 1.4 SE ml/h; and after depletion = 10.4+ 1.0; P < 0.01). We conclude that circulating granulocytes are necessary for the development of increased lung vascular permeability to fluid and protein following endotoxin. The pulmonary vasopressor effects of endotoxin in sheep are independent of granulocytes.

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Section: Resultsmentioning

confidence: 99%

“…We prepared yearling sheep as previously described for collecting lung lymph and measuring vascular pressures (10)(11)(12)(13)(14). Briefly, through three thoracotomies we put catheters into the left atrium, pulmonary artery, and the efferent duct from the caudal mediastinal lymph node.…”

Section: Methodsmentioning

confidence: 99%

Prevention by granulocyte depletion of increased vascular permeability of sheep lung following endotoxemia.

Heflin¹,

Brigham²

1981

J. Clin. Invest.

394

116

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“…A progressive loss of intravascular volume has been documented in dogs treated with endotoxin (409). In sheep, infusion of Pseudomonas strains causes the protein content of the lymph from the lungs to increase (73,74). Similar effects can be obtained in the same animal model administering LPS (72).…”

Section: Absolute Hypovolemiamentioning

confidence: 67%

Cardiovascular Responses During Sepsis

Pecchiari

Pontikis

Alevrakis

et al. 2021

Comprehensive Physiology

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Sepsis is the life-threatening organ dysfunction arising from a dysregulated host response to infection.Although the specific mechanisms leading to organ dysfunction are still debated, impaired tissue oxygenation appears to play a major role, and concomitant hemodynamic alterations are invariably present. The hemodynamic phenotype of affected individuals is highly variable for reasons that have been partially elucidated. Indeed, each patient's circulatory condition is shaped by the complex interplay between the medical history, the volemic status, the interval from disease onset, the pathogen, the site of infection and the attempted resuscitation. Moreover, the same hemodynamic pattern can be generated by different combinations of various pathophysiological processes, so the presence of a given hemodynamic pattern cannot be directly related to a unique cluster of alterations. Research based on endotoxin administration to healthy volunteers and animal models compensate, to an extent, for the scarcity of clinical studies on the evolution of sepsis hemodynamics. Their results, however, cannot be directly extrapolated to the clinical setting, due to fundamental differences between the septic patient, the healthy volunteer and the experimental model. Numerous microcirculatory derangements might exist in the septic host, even in the presence of a preserved macrocirculation. This dissociation between the macro-and the micro-circulation might account for the limited success of therapeutic interventions targeting typical hemodynamic parameters, such as arterial and cardiac filling pressures, and cardiac output. Finally, physiological studies point to an early contribution of cardiac dysfunction to the septic phenotype, however our defective diagnostic tools preclude its clinical recognition.) to anesthetized, vagotomized and mechanically ventilated Sprague-Dawley rats on the operating point of the baroreflex using a baroreflex diagram (SNA: sympathetic nervous activity; CSP: carotid sinus pressure; AP: arterial pressure). As time passes after lipopolysaccharide injection, the neural arc 9 progressively shifts rightwards, and the peripheral arc downwards, so the operating point moves from a (baseline) to b at 1 hour and to c at 2 hours, showing a progressive increase of SNA with little change of AP. From (523), with permission under the terms of the Creative Commons Attribution License. significantly (from 1.7±0.5 to 1.4±0.2 mmHg ml -1 min) (313). In the same preparation N w -nitro-L-methyl ester (L-NAME) increases SVR more than R VR both in the presence (+294 and +129%, respectively) and in the absence (+196 and +107%, respectively) of fluid-loading. In another study from the same group, L-NAME elicited similar effects (117). Overall, these experimental studies warn against the assumption that changes of SVR are always paralleled by similar changes of R VR .

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“…Increases in lymphatic flow were then related to the evolution of two prominent findings in pulmonary edema: perivascular cuffs and alveolar flooding. Studies using a variety of insults, including elevated left atrial pressure (44,116), elevated pulmonary arterial pressure (123), hypoxia and exercise (73,123), chemical toxins (94), inflammatory agents (93), and bacteria or bacterial products (13,14) have documented how increased lymphatic flow related in time to perivascular cuffing and development of alveolar flooding.…”

Section: Studies On the Lung Endotheliummentioning

confidence: 99%

Studies on the cell biology of interendothelial cell gaps

Ochoa

Stevens

2012

American Journal of Physiology-Lung Cellular and Molecular Phys

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Pain, redness, heat, and swelling are hallmarks of inflammation that were recognized as early as the first century AD. Despite these early observations, the mechanisms responsible for swelling, in particular, remained an enigma for nearly two millennia. Only in the past century have scientists and physicians gained an appreciation for the role that vascular endothelium plays in controlling the exudation that is responsible for swelling. One of these mechanisms is the formation of transient gaps between adjacent endothelial cell borders. Inflammatory mediators act on endothelium to reorganize the cytoskeleton, decrease the strength of proteins that connect cells together, and induce transient gaps between endothelial cells. These gaps form a paracellular route responsible for exudation. The discovery that interendothelial cell gaps are causally linked to exudation began in the 1960s and was accompanied by significant controversy. Today, the role of gap formation in tissue edema is accepted by many, and significant scientific effort is dedicated toward developing therapeutic strategies that will prevent or reverse the endothelial cell gaps that are present during the course of inflammatory illness. Given the importance of this field in endothelial cell biology and inflammatory disease, this focused review catalogs key historical advances that contributed to our modern-day understanding of the cell biology of interendothelial gap formation.

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Increased permeability of sheep lung vessels to proteins after Pseudomonas bacteremia

Cited by 24 publications

References 12 publications

Prevention by granulocyte depletion of increased vascular permeability of sheep lung following endotoxemia.

Prevention by granulocyte depletion of increased vascular permeability of sheep lung following endotoxemia.

Cardiovascular Responses During Sepsis

Studies on the cell biology of interendothelial cell gaps

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